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Am J Cardiol. 1992 Oct 08;70(10):113C-118C. doi: 10.1016/0002-9149(92)91368-e.

Angiotensin-converting enzyme inhibition, the sympathetic nervous system, and congestive heart failure. The Australian Zestril (Lisinopril) Study Group.

The American journal of cardiology

G Sloman


  1. Cardiovascular Unit, Epworth Hospital, Richmond, Victoria, Australia.

PMID: 1329466 DOI: 10.1016/0002-9149(92)91368-e


Catecholamines have been found to be powerful indicators of prognosis in patients with congestive heart failure. However, it is uncertain whether catecholamines are a marker for decreased cardiac performance or part of the pathologic process. Catecholamines, exogenously derived beta-adrenergic stimulants, and drugs that amplify sympathetic responsiveness produce early hemodynamic benefits, but do not appear to provide long-term improvement in terms of symptoms or exercise tolerance, whereas blockade of the beta-adrenoceptor appears to have little early benefit but may improve long-term prognosis. This suggests that in the long term, increased catecholamine levels may be deleterious. Angiotensin-converting enzyme (ACE) inhibitors can modulate circulating catecholamines, and the persistence and degree of ACE inhibition may be important not only in reducing catecholamines, but possibly also in reducing mortality in heart failure. It appears that ACE inhibitors definitely reduce mortality in congestive heart failure. It remains to be documented whether the persistence and degree of ACE inhibition is a factor in this effect, and, thus, comparison of short- with long-acting ACE inhibitors and study of the dosage of ACE inhibitors are of importance. The extent to which modulation of the sympathetic nervous system by ACE inhibitors is an important mechanism in their effect in reducing mortality remains to be established.

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